Heart attack is a leading cause of death and results most commonly from an imparment of the blood supply to the heart muscle (myocardium). Oxygen deprivation to the heart muscle, cardiac ischemia, results in impaired function and eventually myocardial cell death and necrosis (infarction). Survival of myocardial infarction victims depends on the extent or size of the infarcted area which has a femoral component. Transformation of cells in the ischemic area from reversibly to irreversibly injured occurs over the course of several hours. Without reperfusion infarct extension continues for up to six hours after the start of an ischemic event. Establishment of reperfusion of the ischemic area stops an evolving myocardial infarction and salvages tissue. However, recent findings suggest that reperfusion of the ischemic tissue with oxygenated blood results in injury caused by oxygen derived free radicals.
2-Oxo- and 2-thioxo-imidazolecarboxamides are known from British Patent number 2,110,668 to possess antiallergy activity. More recently, the antioxidant properties of 2,3-dihydro-5-methyl-2-oxo- and 2-thioxo-1H-imidazole-4-carboxamide and 2,3-dihydro-N,N,5,-trimethyl-2-oxo- and 2-thioxo-1H-imidazole-4-carboxamide were reported by R. C. Smith, et al., Biochemical Pharmacology, 36(9), 1457-1460 (1987). Now it has been discovered that the 2-thioxoimidazolecarboxamides when administered to a patient prior to an ischemic event, during an ischemic event, or during the period of time subsequent to an ischemic event during which reperfusion damage occurs, prevent or lessen the damage which normally occurs when circulation is restored to the portion of the heart formerly deprived of blood.